Normal heart arteries have a muscle tissue layer inside their walls. In coronary artery disease or in response to mechanical injury such as angioplasty (a non-surgical procedure to open clogged arteries), new smooth muscle cells grow along the innermost layer of the arterial lining and leads to narrowing. Such muscle buildup also occurs with use of a stent a small wire mesh tube inserted after angioplasty to keep the artery clear.
It is the most common cause of stent failure, according to Michael Simons, professor of medicine and of pharmacology and toxicology at Dartmouth Medical School and chief of cardiology at Dartmouth-Hitchcock Medical Center, who headed the research team. Based on the research, Simons cautions against using angiogenic drugs to unblock arteries in certain heart conditions. He indicated that stents coated with agents that specifically target smooth muscle to prevent or kill growth should remain the treatment of choice at present. "They are not perfect, so everyone is looking for what can be added to make things better," he noted.
The biological drivers of the smooth muscle accumulation are unclear. Injury may somehow alter the tissue on the inner arterial layer, called the intima, so it is susceptible to factors in the blood that induce smooth muscle cells to proliferate. At the same time, there is an intense inflammatory response on the outermost layer of the arterial wall that also appears to be involved in stimulating blood vessels to feed smooth muscle accumulation.